THE ROLE OF NF-A B IN THE PROTECTIVE EFFECT OF HEAT SHOCK RESPONSE AGAINST CARDIOMYOCYTES INJURY INDUCED BY HYDROGEN PEROXIDE

Shock ◽  
1999 ◽  
Vol 11 (Supplement) ◽  
pp. 32
Author(s):  
Weimin Xiao ◽  
Lia Zhong ◽  
Jialu You ◽  
Zhengyao Luo
Virology ◽  
2010 ◽  
Vol 406 (2) ◽  
pp. 336-341 ◽  
Author(s):  
Yulia V. Lyupina ◽  
Svetlana B. Dmitrieva ◽  
Anna V. Timokhova ◽  
Svetlana N. Beljelarskaya ◽  
Olga G. Zatsepina ◽  
...  

Oncogene ◽  
2003 ◽  
Vol 22 (1) ◽  
pp. 10-27 ◽  
Author(s):  
Yong Xian Ma ◽  
Saijun Fan ◽  
Jingbo Xiong ◽  
Ren-qi Yuan ◽  
Qinghui Meng ◽  
...  

2000 ◽  
Vol 42 (1-2) ◽  
pp. 293-298 ◽  
Author(s):  
R. Pedahzur ◽  
D. Katzenelson ◽  
N. Barnea ◽  
O. Lev ◽  
H.I. Shuval ◽  
...  

The aim of the present work was to evaluate the disinfectant capacity and the possible fields of application of a combined silver and hydrogen peroxide (HP) water disinfectant. The findings demonstrated the high bactericidal action of silver (on E. coli) and its relatively ineffective virucidal effect (on MS-2 phage). HP was found to have a small bactericidal effect and a mild virucidal one. When combined, silver and HP usually exhibited a synergistic action on the viability of E. coli and on the luminescence of recombinant luminescent E. coli. In some instances, the combined bactericidal effects were 1000-fold higher than the sum of the separate ones. No increased virucidal action was observed. The biocidal action of the combination generally increased with increasing temperature and pH, and decreased in secondary and tertiary effluents. The physiological effects and mechanisms of toxicity of HP, silver and their combinations, were assessed by monitoring the induction of stress promoters upon exposure to the active agents, and by assessing the sensitivity of E. coli mutated in major stress responses to HP, silver and their combinations. The results showed that HP induced a wide array of stress responses, that both silver and HP induced promoters regulated by the heat shock response, and that the dnaK promoter (regulated by the heat shock response) was synergistically induced. The mutant sensitivity tests showed that bacteria deficient in the ability to activate central cellular stress responses (SOS, heat shock, stationary phase, oxidative) were hypersensitive to both HP and silver. These results imply that cellular proteins, and possibly the DNA, are the cellular moieties chiefly affected. The above findings suggest that the potentiated effect of HP and silver is a metabolically dependant/related process that stems from a combination and/or accumulation of physiological effects exerted by the active ingredients. The physico-chemical properties of the combined disinfectant, and its disinfection capacity, points to its potential application as a long-term secondary residual disinfectant for water of relatively high quality.


2003 ◽  
Vol 64 (1) ◽  
pp. 85-93 ◽  
Author(s):  
Angela Ianaro ◽  
Armando Ialenti ◽  
Pasquale Maffia ◽  
Paola Di Meglio ◽  
Massimo Di Rosa ◽  
...  

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Marek Andrzej Budzyñski ◽  
Mikael Puustien ◽  
Jenny Joutsen ◽  
Julis Anckar ◽  
Lea Sistonen

2006 ◽  
Vol 84 (5) ◽  
pp. 703-712 ◽  
Author(s):  
Silvia Fossati ◽  
Laura Formentini ◽  
Zhao-Qi Wang ◽  
Flavio Moroni ◽  
Alberto Chiarugi

Poly(ADP-ribose) polymerase-1 (PARP-1)-dependent poly(ADP-ribose) formation is emerging as a key regulator of transcriptional regulation, even though the targets and underlying molecular mechanisms have not yet been clearly identified. In this study, we gathered information on the role of PARP-1 activity in the heat shock response of mouse fibroblasts. We show that DNA binding of heat shock factor (HSF)-1 was impaired by PARP-1 activity in cellular extracts, and was higher in PARP-1−/− than in PARP-1+/+ cells. No evidence for HSF-1 poly(ADP-ribosyl)ation or PARP-1 interaction was found, but a poly(ADP-ribose) binding motif was identified in the transcription factor amino acid sequence. Consistent with data on HSF-1, the expression of heat-shock protein (HSP)-70 and HSP–27 was facilitated in cells lacking PARP-1. Thermosensitivity, however, was higher in PARP-1−/− than in PARP-1+/+ cells. Accordingly, we report that heat-shocked PARP-1 null fibroblasts showed an increased activation of proapoptotic JNK and decreased transcriptional efficiency of prosurvival NF-κB compared with wild-type counterparts. The data indicate that poly(ADP-ribosyl)ation finely regulates HSF-1 activity, and emphasize the complex role of PARP-1 in the heat-shock response of mammalian cells.


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